Six fetal sheep were equipped with intratracheal, amniotic and vascular catheters and electrocorticogram electrodes to study the effect of phenyl isopropyl adenosine (PIA) on electrocorticogram and fetal breathing movements. Three animals had functioning electrocardiogram electrodes. During 1,000-min control periods, low-voltage high- frequency (LVHF) electrocorticogram predominated 60 ± 1 % (mean ± SEM) of total time. Fetal breathing movements occurred 34 ± 1 % of total time and only during LVHF electrocorticogram. PIA 0.125 mg was given intravenously to the fetus during established LVHF electrocorticogram and fetal breathing movements. LVHF electrocorticogram converted in 58 ± 16 s to high-voltage low-frequency (HVLF) electrocorticogram which persisted for 10 ± 3 min. This was followed by a third electrocorticogram pattern for 119 ± 12 min. Fetal breathing movements ceased in 47 ± 25 s and did not recur for 150 ± 20 min. An increase in fetal breathing movements (59 ± 2% of total time) occurred between 300 and 800 min (control 34 ± 1 %, p < 0.05). Electrocardiogram demonstrated a decrease in heart rate from 170 ± 6 to 90 ± 6 beats per min with return to baseline in 113 ± 49 min. No significant changes occurred in blood gases. We conclude that fetal electrocorticogram, fetal breathing movements and heart rate are influenced by adenosine.
Morphine (1 mg/kg) given to the lamb fetus near term induces a significant increase in low-voltage high-frequency (LVHF) electrical activity in the brain. This pattern of the electrocorticogram (ECOG) is associated with simultaneous continuous fetal breathing movements of greater amplitude than control. Naloxone prevents and reverses these morphine-induced changes. The observed phenomena suggest that opiate receptors may play a stimulant role in the control of fetal LVHF ECOG and fetal breathing movements.
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